-
Something wrong with this record ?
Role of histamine receptors in the effects of histamine on the production of reactive oxygen species by whole blood phagocytes
O. Vasicek, A. Lojek, V. Jancinova, R. Nosal, M. Ciz,
Language English Country Netherlands
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Histamine Agonists pharmacology MeSH
- Benzimidazoles pharmacology MeSH
- Dimaprit pharmacology MeSH
- Phagocytes drug effects metabolism MeSH
- Guanidines pharmacology MeSH
- Histamine physiology MeSH
- Humans MeSH
- Methylhistamines pharmacology MeSH
- Reactive Oxygen Species blood MeSH
- Receptors, Histamine H2 metabolism MeSH
- Receptors, Histamine metabolism MeSH
- Receptors, G-Protein-Coupled agonists metabolism MeSH
- Thiourea analogs & derivatives pharmacology MeSH
- Check Tag
- Humans MeSH
- Male MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
AIMS: The diverse physiological functions of histamine are mediated through distinct histamine receptors. In this study we investigated the role of H2R and H4R in the effects of histamine on the production of reactive oxygen species by phagocytes in whole blood. MAIN METHODS: Changes in reactive oxygen species (ROS) production by whole blood phagocytes after treatment with histamine, H4R agonists (4-methylhistamine, VUF8430), H2R agonist (dimaprit) and their combinations with H4R antagonist (JNJ10191584) and H2R antagonist (ranitidine) were determined using the chemiluminescence (CL) assay. To exclude the direct scavenging effects of the studied compounds on the CL response, the antioxidant properties of all compounds were measured using several methods (TRAP, ORAC, and luminol-HRP-H2O2 based CL). KEY FINDINGS: Histamine, 4-methylhistamine, VUF8430 and dimaprit inhibited the spontaneous and OZP-activated whole blood CL in a dose-dependent manner. On the other hand, only VUF8430 was able to inhibit PMA-activated whole blood CL. Ranitidine, but not JNJ10191584, completely reduced the effects of histamine, 4-methylhistamine and dimaprit. The direct scavenging ability of tested compounds was negligible. SIGNIFICANCE: Our results demonstrate that the inhibitory effects of histamine on ROS production in whole blood phagocytes were caused by H2R. Our results also suggest that H4R agonists in concentrations higher than 10(-6)M may also influence ROS production via binding to H2R.
References provided by Crossref.org
- 000
- 00000naa a2200000 a 4500
- 001
- bmc14063717
- 003
- CZ-PrNML
- 005
- 20140709124047.0
- 007
- ta
- 008
- 140704s2014 ne f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.1016/j.lfs.2014.01.082 $2 doi
- 035 __
- $a (PubMed)24530738
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a ne
- 100 1_
- $a Vasicek, Ondrej $u Institute of Biophysics, Academy of Sciences of the Czech Republic, v.v.i., Kralovopolska 135, 612 65 Brno, Czech Republic.
- 245 10
- $a Role of histamine receptors in the effects of histamine on the production of reactive oxygen species by whole blood phagocytes / $c O. Vasicek, A. Lojek, V. Jancinova, R. Nosal, M. Ciz,
- 520 9_
- $a AIMS: The diverse physiological functions of histamine are mediated through distinct histamine receptors. In this study we investigated the role of H2R and H4R in the effects of histamine on the production of reactive oxygen species by phagocytes in whole blood. MAIN METHODS: Changes in reactive oxygen species (ROS) production by whole blood phagocytes after treatment with histamine, H4R agonists (4-methylhistamine, VUF8430), H2R agonist (dimaprit) and their combinations with H4R antagonist (JNJ10191584) and H2R antagonist (ranitidine) were determined using the chemiluminescence (CL) assay. To exclude the direct scavenging effects of the studied compounds on the CL response, the antioxidant properties of all compounds were measured using several methods (TRAP, ORAC, and luminol-HRP-H2O2 based CL). KEY FINDINGS: Histamine, 4-methylhistamine, VUF8430 and dimaprit inhibited the spontaneous and OZP-activated whole blood CL in a dose-dependent manner. On the other hand, only VUF8430 was able to inhibit PMA-activated whole blood CL. Ranitidine, but not JNJ10191584, completely reduced the effects of histamine, 4-methylhistamine and dimaprit. The direct scavenging ability of tested compounds was negligible. SIGNIFICANCE: Our results demonstrate that the inhibitory effects of histamine on ROS production in whole blood phagocytes were caused by H2R. Our results also suggest that H4R agonists in concentrations higher than 10(-6)M may also influence ROS production via binding to H2R.
- 650 _2
- $a benzimidazoly $x farmakologie $7 D001562
- 650 _2
- $a dimaprit $x farmakologie $7 D017259
- 650 _2
- $a guanidiny $x farmakologie $7 D006146
- 650 _2
- $a histamin $x fyziologie $7 D006632
- 650 _2
- $a agonisté histaminu $x farmakologie $7 D017442
- 650 _2
- $a lidé $7 D006801
- 650 _2
- $a mužské pohlaví $7 D008297
- 650 _2
- $a methylhistaminy $x farmakologie $7 D008761
- 650 _2
- $a fagocyty $x účinky léků $x metabolismus $7 D010586
- 650 _2
- $a reaktivní formy kyslíku $x krev $7 D017382
- 650 _2
- $a receptory spřažené s G-proteiny $x agonisté $x metabolismus $7 D043562
- 650 _2
- $a receptory histaminu $x metabolismus $7 D011968
- 650 _2
- $a receptory histaminu H2 $x metabolismus $7 D011970
- 650 _2
- $a thiomočovina $x analogy a deriváty $x farmakologie $7 D013890
- 655 _2
- $a časopisecké články $7 D016428
- 655 _2
- $a práce podpořená grantem $7 D013485
- 700 1_
- $a Lojek, Antonin $u Institute of Biophysics, Academy of Sciences of the Czech Republic, v.v.i., Kralovopolska 135, 612 65 Brno, Czech Republic.
- 700 1_
- $a Jancinova, Viera $u Institute of Experimental Pharmacology & Toxicology, Slovak Academy of Sciences, Dubravska cesta 9, 841 04 Bratislava, Slovak Republic.
- 700 1_
- $a Nosal, Radomir $u Institute of Experimental Pharmacology & Toxicology, Slovak Academy of Sciences, Dubravska cesta 9, 841 04 Bratislava, Slovak Republic.
- 700 1_
- $a Ciz, Milan $u Institute of Biophysics, Academy of Sciences of the Czech Republic, v.v.i., Kralovopolska 135, 612 65 Brno, Czech Republic. Electronic address: milanciz@ibp.cz.
- 773 0_
- $w MED00003147 $t Life sciences $x 1879-0631 $g Roč. 100, č. 1 (2014), s. 67-72
- 856 41
- $u https://pubmed.ncbi.nlm.nih.gov/24530738 $y Pubmed
- 910 __
- $a ABA008 $b sig $c sign $y a $z 0
- 990 __
- $a 20140704 $b ABA008
- 991 __
- $a 20140709124339 $b ABA008
- 999 __
- $a ok $b bmc $g 1031201 $s 862449
- BAS __
- $a 3
- BAS __
- $a PreBMC
- BMC __
- $a 2014 $b 100 $c 1 $d 67-72 $i 1879-0631 $m Life sciences $n Life Sci $x MED00003147
- LZP __
- $a Pubmed-20140704
